Chap 6- Immune System Flashcards
1
Q
What are the cell types of the immune system?
A
- lymphocytes
- antigen-presenting cells
- effector cells
2
Q
what kind of cells make up lymphocytes?
A
B and T cells
3
Q
what are them main antigen- presenting cells?
A
- dendritic cells
- macrophages
4
Q
what are the main effector cells?
A
- T lymphocytes
- Macrophages
- Granulocytes
5
Q
Dendritic cells
A
- strong antigen- presenting cells
- expand innate response and elicit adaptive immunity
- secrete cytokines that activate NK cells and differentiate T cells
6
Q
What kind of cells are CD4+ cells?
A
helper T cells
7
Q
What kind of cells are CD8+ cells?
A
Cytotoxic T cells
8
Q
natural killer cells (NK)
A
- kills pathogens inside the cell
- respond to IL-2 and secrete INF- gamma which activate macrophages
9
Q
What is the main function of lymphocytes?
A
produce antibodies, neutralize pathogen, phagocytosis, complement activation
10
Q
what is the main function of helper T cells?
A
activate macrophages, activate other T and B cells
11
Q
what are MHC complex’s?
A
- Major histocompatibility complex
- proteins on antigen- presenting cells that present antigen to T cells
- genes located on chromosome 6
12
Q
what is human MHC proteins?
A
- human leukocyte antigens (HLAs)
- MHC is shared throughout all mammals, HLAs are specific to humans
13
Q
What are Class II MHC cells?
A
- CD4+ helper T lymphocytes interact with dendritic cells and macrophages, activate CD4+ cells
- located on antigen- presenting cells
- is the more sophisticated class
14
Q
What are Class I MHC cells?
A
- present in all nucleated cells
- CD8+ activated to kill any type of virus- infected cell
15
Q
what are the generative lymphoid organs?
A
thymus and bone marrow
16
Q
what are the peripheral lymphoid organs?
A
lymph nodes, spleen, mucosal and cutaneous lymphoid tissues
17
Q
lymphocyte recirculation
A
- most important for T cells
- T cells need to come to lymph nodes where they are activated and differentiated
- can then go to peripheral tissues
- B cells do not need to do this- can go anywhere
18
Q
why are the lymph nodes important?
A
collect antigens from tissue
19
Q
why is the spleen important?
A
captures blood- borne antigens by antigen- presenting cells in the spleen
20
Q
what is the first line of defense?
A
- external defense
- physical barriers like skin, mucus, nasal hair
- chemical barrier like oil, sweat, stomach pH
- type of innate immunity
21
Q
what is the second line of defense?
A
- inflammation
- phagocytes: macrophages and neutrophils
- fever
- complement system
- NKC
- type of innate immunity
22
Q
What is the third line of defense?
A
- active immunity
- passive immunity
- both are types of acquired immunity
23
Q
what is active immunity?
A
- immunity that is cell mediated (T or B cells)
- your body makes antibody when exposed to antigen
24
Q
What is passive immunity?
A
antibody artificially produced outside is directly injected into the body
25
what happens during innate immunity?
- inflammation
- antiviral mechanisms
- functions of epithelia
- innate immunity is non-specific
26
What is the role of Type I IFN?
virus infects a cell -> cell produces type I IFN -> does not allow virus to make protein/ degrades genetic material -> virus dies
27
What are the functions of epithelia in innate immunity?
- physical barrier to infection- most pathogens cannot pass
- kill microbes by locally producing antibiotics
- kill microbes and infected cells by intraepithelial lymphocytes (limited specificity)
28
what is defensin?
a type of antibiotic made by the epithelium
29
what happens during adaptive immunity?
- humoral immunity
| - cellular immunity
30
what is humoral immunity mediated by?
B cells and antibodies
31
what is cellular immunity mediated by?
T cells
32
what is the innate immunity mechanism?
- ready to react to pathogens
- not specific to any particular pathogen
- works in first 6-12 hours of infection
33
what is the adaptive immunity mechanism?
- stimulated by microbes and non-microbial substances
- works within 1-5 days after infection
- results in very specific responses
34
innate immunity receptors
- recognize PAMPs and DAMPs
- can respond to any type of microbe
- receptors are not diverse
- receptors are non- clonal
- innate immunity does not harm healthy cell
35
adaptive immunity receptors
- have different microbes with specific receptors for each
- many different receptors due to genetic changes
- receptors are specific to an antigen
- more likely to cause autoimmune diseases
36
how does the binding of an antibody inactivate antigens?
- neutralization- bind to important parts of microbe so it cannot be recognized by receptor, more easily phagocytized
- agglutination- glue microbes together so easier to phagocytize
- precipitation of antigen- form long chain and precipitate out of solution to be more easily phagocytized
- activate complement system
37
how do naive B cells become mature?
- naive B cells have not encountered any pathogens
- produce IgM
- once B cells introduced to microbe with help of helper T cells, start to proliferate/differentiate
- can differentiate into different classes of immunogloblulins
38
Ig Class switching
- B cells go through class switching with the help of helper T cells
- IgM -> IgG, IgE or IgA depending on situation
39
IgM
complement activation
40
IgG
- neonatal immunity
| - passes through placenta to fetus
41
IgE
- allergic reaction
- Helminths
- found on mast cells who produce histamines
42
IgA
antibody in mucus, tears, saliva
43
affinity maturation
- want B cells anitibodies to have a very high affinity for anitgen
- subgrouped into T depended and T independent
44
T- dependent affinity maturation
- helper T cells help B cells to do class switching
- have high affinity for antibodies
- long-lived
45
T- independent affinity maturation
- results in IgM
- low affinity antibodies
- short- lived
46
primary antibody response
- 5- 10 day lag time
- peak response is small
- usually produces IgM to IgG
- Lower affinty
47
Secondary antibody response
- repeated infection
- 1-3 day lag time
- large peak response
- increase in IgG, in some situations can have class switching as well (higher affinity)
48
migration of T cells
- naive T cells migrate from blood into lymph nodes
- in lymph nodes T cells activated by antigens
- Activated T cells leave nodes, enter blood stream, migrate to peripheral tissues
49
acute viral infections
- CD8+ T cells proliferate and differentiate into effector cytotoxic T cell and memory cells
- clear virus
50
chronic viral infection
- CD8+ cells initially respond
- there is a response, but does not last as long because inhibitory receptors are expressed
- virus is able to persist
51
what is hypersensitivity?
- excessive, uncontrolled or misdirected immunological reaction
- occurs in allergic reactions or autoimmune diseases
52
what triggers hypersensitivity?
exogenous or endogenous antigens
53
atopy
increased susceptibility to develop hypersensitivity reaction
54
atopy
increased susceptibility to develop hypersensitivity reaction
55
Hypersensitivity Type I
- allergen introduced
- Helper T cells activated, stimulate B cells to make IgE
- IgE binds to receptor on mast cell -> sensitized
- activated mast cell secretes vasoamines and lipid mediators (histamine and serotonin) , cytokines
56
what is the immediate response to hypersensitivity I?
- release of histamine and serotonin
- vasodilation
- vascular leakage
- smooth muscle spasm
- caused by prostaglandins and leukotriens, histamines, proteases
57
clinical examples of type I hypersensitivity
- allergic rhinitis
- food allergy
- bronchial asthma
- anaphylaxis
58
what is the late phase reaction of hypersensitivity I reactions?
- leukocyte infiltration
- epithelial damage
- bronchospasm
- caused by cytokines and chemokines
- occures 2-24 hours after
59
what is a hypersensitivity type II reaction?
- antibody mediated diseases- anything except IgE
| - can be caused by opsonization and phagocytosis, complement system, or antibody- mediated cellular dysfunction
60
What is a hypersensitivity type III reaction?
- antigen- antibody complex is formed
- antigen- antibody complex deposited in various tissues
- immune complex- mediated inflammation and tissue injury occurs i.e. fever, joint pain, lymph node enlargement
61
clinical examples of type III hypersensitivity reactions
- systemic lupus erythematosus
| - reactive arthritis
62
What is a hypersensitivity type IV reaction?
- has nothing to do with B cells or antibodies
- mediated by T cells
- CD4+ mediated inflammation: delayed, secrete cytokines that stimulate inflammation and activate phaygocytes, inflammation and tissue injury occurs
- CD8+ directly kill cells by perforins and granzymes
63
perforins
enzyme inside T cell, produces pores
64
granzymes
lysing enzyme
65
clinical examples of hypersensitivity type IV reactions
- type 1 diabetes
- contact sensitivity
- Tb
66
autoimmune disease
- loss of self-tolerance
- involves both T and B cell responses
- body naturally produces reactive b and t cells that are reactive, body has tolerance to these reactive cells in healthy people
67
are autoimmune diseases seen more often in men or women?
women
68
what is central tolerance?
- occurs in thymus and bone marrow
| - reactive lymphocytes go through apoptosis, receptor editing, or dev of regulatory T lymphocytes
69
what is receptor editing?
b cells change their receptor specificity through genetic modifications
70
peripheral tolerance
- regulatory t lymphocytes surpress reactive t or b lymphocytes
- anergy occurs
71
what is anergy?
- occurs in peripheral tissues
| - lymphocyte recognizes antigens but are functionally unresponsive due to lack of co-stimulating signals
72
what do costimulators do?
cause self tolerance failure on antigen presenting cells
73
what is molecular mimicry?
- occurs in T and B cells
- T cells recognize microbial agent which is similar to self antigen
- results in cross reaction and T cells are activated
- Tissue is damaged
74
systemic lupus erythematosus
- autoimmune diseases
- blood serum has autoantibodies, especially antinuclear antibodies (ANA)
- Anti-Sm is specific type of autoantibody associated with SLE
- cause is deposition of immune complexes and binding of anitbodies to cells and tissues
75
SLE Etiology
- genetic factors
- defective elimination of self reactive B cells
- ineffective peripheral tolerance mechanism
- UV light inducing apoptosis, promotes inflammation
76
clinical manifestations of SLE
- usually young woman
- butterfly rash!!
- hematologic symptoms
- arthritis
- fever
- fatigue
77
graft
healthy tissue taken from one part of the body to replace diseased or injured tissue removed from another part of the body
78
autograft
transfer of tissue from one location of persons body to another
79
isograft
transplantation between two genetically identical individuals (twins)
80
allograft
- aka homograft
- transplant of organ or tissue that comes from another person of same species
- most common type of graft
81
xenograft
transfer of tissue or organ between members of different species
82
alloantigen
- antigen of allograft and main target of rejection
| - proteins encoded by MHC
83
allorecognition
- donor antigen presenting cells present graft via MHC II to patient T cells
- recipient antigen presenting cell uptake alloantigen, present it to its own T or B cells
84
transplant sensitization
- graft antigens expressed on donor dendritic cells transported to peripheral lymphoid organs
- alloantigen specific T cells activated
85
Transplant Rejection
- T cells migrate back into graft and destroy graft cells
| - cytokines are produced against graft antigen
86
mechanisms of graft rejection
- hyperactive rejection
- acute rejection
- chronic rejection
87
hyperactive rejection
- circulating alloantigen binds to surface of endothelial cell
- complement sys activated, inflammation, and thrombosis
- occurs almost immediately after transplant
88
acute rejection
- months after transplant
| - cytotoxic T cells react with endothelial cells, cause inflammation aka endothelialitis
89
chronic rejection
- years after rejection
- occurs if patient stops immunosuppressive therapies
- progressive issue that is normally controlled through immunosuppressives
- causes fibrosis and vessel occlusion (graft arteriosclerosis)
90
primary immunodeficiency
- hereditary
- manifests between 6 mo to 2 years
- can be innate or adaptive deficiency
91
secondary immunodeficiency
- due to infections, malnutrition, aging, immunosuppression, autoimmunity, and irradiation/chemotherapy
92
HIV/ AIDS
- HIV-1 main cause in US
- virus contains RNA
- enzyme has reverse transcriptase that makes DNA from RNA
- most drugs target reverse transcriptase
93
HIV transmission
- sexual contact
- IV drug use
- vertical transmission (mother -> child)
94
stage 1 of HIV infection
- acute stage
- 2-4 weeks after infection
- flu like symptoms
95
Stage 2 of HIV infection
- clinical latency
- HIV has low low level of virus production- doesnt proliferate at high level
- chronic HIV infection may take years
- CD4 cell counts decrease
96
stage 3 of HIV infection
- AIDS
- almost no CD4
- virus levels very high
- daignosis based on CD4 count
